Childhood Onset Schizophrenia (COS) is known to result in a more severe and debilitating form of schizophrenia. It is rare, but often studied, as researchers try to look at the factors that lead to the adult disease, focusing on the neurodevelopmental theory. They have looked at overall development of children born to parents who have schizophrenia. They have looked at the frequency of obstetrical complications in individuals with schizophrenia. They have looked at the brain development of those with COS as compared to adolescents and adults. In each area they find clues to the reasons behind this illness. It is fascinating to see how many early events have a part in the development of this disease.
Even before childhood, at birth these individuals seem to have factors that are part of their eventual development of schizophrenia. Cannon has postulated that obstetrical complications combined with genetic factors lead to schizophrenia. He has found that early onset schizophrenia (EOS) is 7.30 times more likely to have had hypoxic obstetrical complications than those with adult onset. This can contribute to the early brain lesion that researchers feel is ultimately behind the development of schizophrenia. Cannon also proposes that this earlier onset in COS allows for an earlier and more robust pruning of synapses during adolescence – “variations in the rate of synaptic pruning would vary the age of clinical onset of schizophrenia” (Cannon 2000).
In terms of development, there have been studies that look back at the early lives of people with schizophrenia to see if there are any early signs that might give a clue as to who will develop the disease. In interviewing parents, it has been found that those who go on to develop schizophrenia have delayed speech milestones, difficulty in reading and writing, and greater overall developmental deviance. They show poor premorbid adjustment in childhood. Particularly boys show even more as they move through adolescence. There are cognitive deficiencies and some motor difficulties. Finally, they show more Schizophrenia Spectrum trait (Hollis 1995). What’s particularly interesting is that they have found more impairment in COS than in even EOS. One study by Vourdes has shown a 19.4% delay in language and speech in COS as compared with EOS. They also found that schizophrenia spectrum traits were more pronounced in COS. They exhibited more deviance in bizarre ideas and perceptions, more of a restricted affect and odd speech (Vourdes 2003). Nicholson has found that there is a much higher incidence of PDD in children that go on to develop COS. 25% of those with COS had a premorbid PDD, showing a social impairment most predominantly, he reports that PDD in COS is more likely to be a marker of severe early abnormal neurodevelopment (Nicholson 2003). So, there are significant early markers for this illness. These could in fact lead to earlier diagnosis, before the devastating symptoms emerge and then maybe earlier treatment that might prevent some of the brain destruction.
Moving into the more specific changes that are found in the brains of adolescent and COS. Thompson took a cohort of COS and took 3 MRI’s at 2 year intervals to see the progression of brain changes between childhood through adolescence “Over 5 years, these deficits progressed anteriorly into temporal lobes, engulfing sensorimotor and dorsolateral prefrontal cortices, and frontal eye fields. These emerging patterns correlated with psychotic symptom severity and mirrored the neuromotor, auditory, visual search, and frontal executive impairments in the disease” (Thompson 2001). Researchers are trying to connect symptoms to brain areas and finding some correlations. This has been attempted over the years, but it seems they are finally finding some real connections. It was also found that in some areas of the brain the tissue loss was faster the younger the client was and that the faster there was tissue loss, the more severe the symptoms.
Coming at this from another angle – looking at the loss of grey matter in COS Gogtay compared COS with children with atypical psychosis. Gogstay suggests that there is a diagnostically specific GM volume loss in COS that was not seen in children with atypical psychosis. “An ongoing neurodevelopmental process and/or brain response specific to the illness could account for these changes.” (Gogtay 2004)
There are a number of factors that all seem to play into the development of schizophrenia from a very early age. Comparing the neurodevelopment of those with the more severe COS with those without yields much interesting data. (Rapoport 2004) It seems to point to an element – genetic – that is then compounded by environmental effects. The maturing brain then adapts to this maladaptation and develops in specific patterns the symptoms. The more we can learn about the early indicators of this illness, the closer we can get to the root causes. Interesting work is being done on looking at all these factors as they relate to the interconnectivity of the disorder. It is clearly not one gene or birth insult or developmental pattern. It is rather the interplay of all these factors that will lead into understanding more fully the causes and development of this devastating disease.
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